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Acquired bartter-like syndrome associated with gentamicin administration
Chu-Lin Chou1, Yeong-Hwang Chen, Tom Chau
1Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
The American Journal of the Medical Sciences
|March 16, 2005
Summary
Gentamicin therapy can cause acquired Bartter-like syndrome, a condition with electrolyte imbalances. This syndrome, characterized by hypokalemia and hypocalcemia, typically resolves after gentamicin cessation and electrolyte supplementation.
Area of Science:
- Nephrology
- Pharmacology
- Endocrinology
Background:
- Aminoglycoside antibiotics, like gentamicin, are known for nephrotoxicity.
- Acquired Bartter-like syndrome is a less recognized adverse effect of gentamicin treatment.
Observation:
- Four female patients developed paresthesia, muscle weakness, and tetany after gentamicin therapy.
- Patients exhibited hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalcemia.
- Low parathyroid hormone levels were observed despite hypocalcemia.
Findings:
- Biochemical profiles were consistent with Bartter-like syndrome, including renal wasting of electrolytes (Na+, K+, Cl-, Ca2+, Mg2+).
- These abnormalities resolved within 2–6 weeks after gentamicin cessation with supportive care.
- The observed electrolyte disturbances mimicked those seen in calcium-sensing receptor gain-of-function mutations.
Implications:
- Gentamicin may induce Bartter-like syndrome by activating the calcium-sensing receptor in renal tubules.
- This highlights a novel mechanism of aminoglycoside-induced nephrotoxicity.
- Clinicians should consider monitoring electrolytes in patients receiving gentamicin, especially those with neurological symptoms.